姜黄素预防高原缺氧大鼠认知功能障碍的电生理机制

The Electrophysiology Mechanism of Curcumin Prevent Hypobaric Hypoxia-Induced Cognitive Deficits

目的:探讨姜黄素(curcumin)预防高原缺氧大鼠认知功能障碍的电生理机制。方法:将30只成年雄性SD大鼠随机分为健康对照组、模型组(Model组)、姜黄素[按体重60mg/(kg.d)]治疗组(curcumin组)。造模后,检测脑片水平的海马的LTP变化,并运用膜片钳技术检测海马CA1区神经元的电生理变化。结果:(1)给予HFS刺激后各组均可诱发LTP并持续1h以上,与对照组比较模型组组HFS刺激后LTP明显被抑制(P<0.05),姜黄素可减轻缺氧所致的LTP抑制(P<0.05);(2)高原缺氧使海马CA1神经元阈电位升高,动作电位(AP)数量减少,兴奋性降低,姜黄素干预可明显减轻高原缺氧对细胞神经元的抑制。结论:姜黄素可显著改善高原缺氧大鼠认知功能障碍,其可能机制是通过维持海马CA1细胞的兴奋性减轻高原缺氧对认知功能的损伤。

Objective： To investigate the electrophysiology mechanism of curcumin prevent hypobaric hypoxia -induced cognitive deficits. Methods： 30 male Sprague-Dawley rats（200± 20 g） were randomly divided into three groups with 10 rats in each group： Control group, Model group and Curcumin group. Hippocampal LTP was detected by electrophysiology method. Excitability of Hippocampal CA1 neuron was measured by whole-cell patch-clamp recordings in rat brain slices. Results： LTP inhibition in hippocampus caused by hypobaric hypoxia are markedly improved by administration of curcumin. The excitability of hippocampal CA 1 neurons is inhibitted by hypobaric hypoxia, and curcumin can maintain the excitability of neuron. Conclusions： Curcumin can prevent hypobaric hypoxia-induced cognitive deficits through maintain the excitability ofhippocampal CA1 neurons.